Patients having severe congestive heart failure (CHF), such as class III and IV on the New York Heart Association (NTHA) scale, may become refractory, i.e., resistant, to standard medical therapy. One factor which may contribute to such resistance is renal insufficiency with renal perfusion.
A number of device-based therapies have been developed to prevent the progression of heart failure and to improve systolic function in patients suffering from CHF, as is well known to those of ordinary skill in the art. One therapy is cardiac resynchronization therapy (CRT), which has proven to be an effective method to decrease morbidity and mortality, and to increase quality of life in patients with severe to moderate heart failure and mechanical dyssynchrony. The implantation of a biventricular pacemaker in such patients leads to a more synchronous, simultaneous contraction pattern of the right and left ventricles, and, assuming proper placement of the ventricular pacing lead and optimized pacemaker settings, results in an improvement in systolic performance of the heart, which can be measured as improvements in left ventricular ejection fraction, end-diastolic volume, end-systolic volume, and end-diastolic pressure. So called reverse remodeling may not only be achieved by CRT, but also through other methods, depending on the underlying root cause for the severe systolic dysfunction and the benefit those methods offer with respect to the treatment of those specific root causes, left ventricular assist devices (LVAD) for patients with severely failing hearts who are waiting for heart transplants, cardiac contractility modulation (CCM) with very low systolic strength and no dyssynchrony, and external counter pulsation therapy (ECPT) to name a few conditions.
While cardiac rhythm management devices, e.g., CRT, are proven effectively to improve systolic function, electrical stimulation of the heart through internal electrodes, however, may also cause unwanted stimulation of skeletal muscle.
Referring briefly to FIG. 1, a patient's chest cavity is depicted generally at 10. In cavity 10 is contained the patient's heart 12, right lung 14 and left lung 16. The left phrenic nerve 18, which provides innervation for the diaphragm 20, arises from the cervical spine and descends to diaphragm 20 through the mediastinum 22 where the heart is located. As it passes heart 12, left phrenic nerve 18 courses along the pericardium 24, superficial to the left atrium 26 and left ventricle 28. Because of its proximity to any electrodes used for pacing, the phrenic nerve may be stimulated by a pacing pulse, i.e., phrenic nerve stimulation (PNS), The resulting involuntary contraction of the diaphragm may be quite annoying to the patient, resulting in a spasm similar to a hiccup. PNS has been reported in about a quarter of patients having implanted CRT devices.
PIDS/PNS is intended to cause contraction of the diaphragm, and may be accomplished by an invasive implantation of electrode(s), may be accomplished by stimulation through percutaneous pathways, or by placement of electrodes on the surface of the human body.
While PIDS/PNS may have painful side effects and other undesirable symptoms, it remains an effective tool for controlling respiration, for providing utility in the acute and chronic treatment of breathing disorders, and for controlling respiration during medical procedures. A diaphragmatic pacemaker is described in U.S. Pat. No. 5,056,519 for Unilateral diaphragmatic pacer to Vince, granted Oct. 15, 1991.
Other uses of implantable or cutaneous-based medical stimulations devices are known to those of ordinary skill in the art.